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Specific guide to this web site for:
1. Medical
School
Educators
in
Statistics
2. Medical Students
3. Science media writers
4. High School & College
Statistic Teachers
Misadventures:
1. Harvard led MI study
2. JACC
study
(J. of Amer. Coll.
Cardio.)
3. NEJM
cath study
4. Amer. J. of Cardio.
review of literature
5. ALLHAT
controversy
6. Oat bran study
7. Pregnancy & Alcohol
8. Are Geminis
really
different?
9. Columbia 'Miracle' Study
Additional
Topics:
Celebrex
Limitations of Meta-Analyses
Large Randomized Clinical
Trials
Tale of Two Large
Trials
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meta-analyses
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An article was published by
Dabaghi1, et al, evaluating
the effects of low dose aspirin on platelets. Though the data their experiment generated was valid, their conclusions
were erroneous because of an incorrect review of the literature in the article.
Their experimental data showed that a low dose of aspirin (81 mg)
completely inhibited the aggregation of platelets when a particular type of
stimulus was tested (a thromboxane stimulus which is a particular type of
prostaglandin). They incorrectly misinterpreted prior studies as suggesting the
results of other more potent stimulators of platelet aggregation such as
epinephrine or collagen, which is a component of connective tissue, had similar
effects to thromboxane.
There was one trial they could not explain which was an
eloquent study reported in the journal of Prostaglandins by Kastor et al2, which showed that a
single low dose aspirin did not fully inhibit platelets when a collagen stimulus
was used. When Robert Roberts, M.D.,
a distinguished academician and one of the authors of this paper, presented some
information shortly after this paper was published, he stated his group thought
a single low dose of aspirin completely inhibited platelets.
In response to a question about the prostaglandin study by Kastor, et al2,
he said his group thought that the prostaglandin study may have used a faulty
platelet aggreganometer (a device that measures platelet aggregation) to explain
why that study’s results were different than their understanding of the other
trial results.
The Dabaghi
paper1
reached erroneous conclusions because of incorrectly reviewing the previously
performed studies. Quite appropriately Dabaghi et al1 did state that further investigation was needed before low
dose aspirin could be advocated in the use of acute ischemic syndromes because they studied normal patients
and not patients with a threatened heart attack.
There was the
potential though for other individuals to see this paper and not appropriately limit
applying this information before further studies were performed.
The review of literature in the
Dabaghi
article was factually incorrect. All the
prior data for platelet aggregation was consistent. A single low dose of aspirin
does not give the full effects of aspirin on platelet inhibition even in normal
subjects. The Kastor study in Prostaglandins2 has actually
previously generated data on thromboxane precipitated
aggregation that the Dabaghi article reliably recreated.
The review of literature was done incorrectly. Therefore, it was not
apparent to Dabaghi et al that while thromboxane platelet aggregation was inhibited by low dose
aspirin, a single low dose of aspirin did not reliably inhibit the more intense
platelet stimulation that occurred with collagen or epinephrine (epinephrine is
an adrenaline-like substance).
1.
Effects of Low-Dose Aspirin on In Vitro Platelet Aggregation in the Early
Minutes After Ingestion in Normal Subjects. Dabaghi S, Kamat S, Payne J,
Marks G, Roberts R, Schafer A, Kleiman N. Am J Cardiol 1994;
74:720-733
2 Kuster L,
Frolich J. Platelet aggregation and thromboxane release induced by arachidonic acid,
collagen,
ADP, and platelet-activating factor following low
dose acetylsalicylic acid in man. Prostaglandins 1986;32:415-423
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